Objective: To observe the change in the expression of uncoupling protein 2 (UCP2) in kidney mitochondria in rats with hypothyroidism, and study the mechanism of renal injury due to hypothyroidism.
Methods: The Wistar rats were randomly divided into control group (n=10) and hypothyroidism group (n=10). The hypothyroidism rat model was reproduced by low-iodine diet. The intake of iodine in control group and hypothyroidism group were 10.00 μg/d and 1.24 μg/d, respectively. The rats were raised under these conditions respectively for 3 months after they adapted to the feeding for 1 week. Then the thyroid function parameters were measured in blood, and the expressions of UCP2 protein and mRNA in renal tissue were measured by immunohistochemistry and reverse transcription-polymerase chain reaction (RT-PCR) methods.
Results: The thyrotropic-stimulating hormone (TSH, mU/L) in hypothyroidism group was significantly higher than that in control group (4.88±1.37 vs. 1.65±0.33, P<0.05). The levels of total triiodothyronine (TT(3)), total thyroxine (TT(4)), free triiodothyronine (FT(3)) and free thyroxine (FT(4)) in serum in hypothyroidism group were significantly lower than those in control group [TT(3) (nmol/L) : 0.54±0.07 vs. 0.98±0.17, TT(4) (nmol/L): 7.82±2.18 vs. 48.78±3.65, FT(3) (pmol/L): 2.28±0.22 vs. 2.99±0.10, FT(4) (pmol/L): 11.38±1.74 vs. 29.27±0.95, all P<0.01]. The immunohistochemistry study revealed that the UCP2 protein expression in both renal glomeruli and tubule tissues in the hypothyroidism group was significantly lower than that of control group (renal glomeruli: 0.17±0.02 vs. 0.24±0.04, renal tubule: 0.19±0.02 vs. 0.25±0.02, both P<0.01). The RT-PCR showed that the UCP2 mRNA expression in the hypothyroidism group was significantly lower than that of control group (0.70±0.19 vs. 1.30±0.09, P<0.01).
Conclusion: Hypothyroidism may produce damage to kidney, which is related to the down-regulation of UCP2 expression in the mitochondria of renal cells.